The effects of zearalenone (ZEA), an estrogenic mycotoxin produced by Fusarium fungi, on bovine neutrophils were investigated in vitro using chemiluninescence, a bactericidal parameter. ZEA suppressed luminol-dependent, phorbol 12-myristate 13-acetate (PMA)-elicited chemiluminescence in a dose-dependent manner at concentrations of 10(-4) M and 10(-5) M. No significant suppression was observed at concentrations lower than 10(-6) M. The possible mode ofaction of 10(-4) M ZEA on the cell activity was investigated with special reference to intracellular Ca2+ ([Ca2+]i) release and estrogen receptors. The 10(-4) M ZEA treatment significantly impaired [Ca2+]i release. When pretreated with a low dose (10(-6) M) of PMA, the cells resisted the ZEA-induced chemiluminescence suppression. However, pretreatment of the cells with the estrogen receptor blockers Tamoxifen and ICl 182,780 (both at 10(-6) M) did not annul the suppressive ZEA action. Considering that PMA is an activator of protein kinase C (PKC), a signal transducing enzyme, and in association with a rise in [Ca2+]i causes cytosolic PKC to shift to the plasma membrane where the activated PKC triggers a varied array of cellular responses, the pharmacological dose of ZEA might have suppressed chemiluminescence by hindering the release of [Ca2+]i and the PKC shift. The results of pretreatment with estrogen receptor blockers, however, did not support the suggestion that the ZEA treatment affected the cells via estrogen receptor pathways.